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Typus
KomplettPlagiat
Bearbeiter
Graf Isolan
Gesichtet
Yes.png
Untersuchte Arbeit:
Seite: 11, Zeilen: 1-15
Quelle: Gorji 2005
Seite(n): 27, Zeilen: left col. 6ff
SD is a well-known phenomenon in experimental epilepsy. SD has been observed in a variety of in vitro and in vivo epilepsy models in different animal species. Reduction of extracellular Mg2+ concentrations, activation of NMDA receptors, blocking of K+ channels, e.g., by 4-aminopyridine, increased extracellular K+, blocking of Na+–K+ ATPase, e.g., by ouabain, blocking of Ca2+ channels, e.g., by NiCl2, blocking of GABA receptors, e.g., by picrotoxin, are the common pathways for eliciting epileptiform burst discharges and SD in experimental models (Gorji, 2001). By all aforementioned mechanisms SD appears spontaneously between epileptiform ictal events. SD can be elicited in susceptible area by a single discharge of an epileptic focus (spike triggered SD). Epileptiform field potentials usually suppress during SD occurrence and reappear in few minutes (Koroleva and Bures, 1983). CSD penetration into epileptic foci established in different models of epilepsy. However, it should be noted that SD does not enter electrically or pharmacologically elicited foci of epileptic activity with high rates of interictal discharges which resulted in anomalous SD propagation. This abnormal SD conduction may account for periodic changes of ictal and interictal activity found in some types of focal epilepsy (Koroleva and Bures, 1983). SD is a well known phenomenon in experimental epilepsy. SD has been observed in a variety of in vitro and in vivo epilepsy models in different animals species. Reduction of extracellular Mg2+ concentrations, activation of NMDA receptors, blocking of K+ channels e.g. by 4-aminopyridine, increased extracellular K+, blocking of Na+-K+ ATP-ase e.g. by ouabain, blocking of Ca2+ channels e.g. by NiCl2 , blocking of GABA receptors e.g. by picrotoxine are the common pathways for eliciting epileptiform burst discharges and SD in experimental models (Leao 1944A, Petsche et al. 1973, Traynelis and Dingledine 1988, Psarropoulou and Avoli 1992, Balestrino et al. 1999, Gorji et al. 2003A). By all aforementioned mechanisms SD appears spontaneously between epileptiform ictal events. SD can be elicited in susceptible area by a single discharge of an epileptic focus (spike triggered SD). Epileptiform field potentials usually suppress during SD occurrence and reappear in few minutes (Koroleva and Bures 1983, Gorji et al. 2000). CSD penetration into epileptic foci established in different model of epilepsy. However, it should be noted that SD does not enter electrically or pharmacologically elicited foci of epileptic activity with high rates of interictal discharges which resulted in anomalous SD propagation. This abnormal SD conduction may account for periodic changes of ictal and interictal activity found in some types of focal epilepsy (Koroleva and Bures 1980, Bures et al. 1975).
Anmerkungen

Nothing is marked as a citation.

Can also be found in Quelle:Clg/Gorji 2001.

Sichter
(Graf Isolan) Schumann

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